Clozapine Withdrawal Resulting in Delirium With Psychosis

Stanilla, Joseph K.; León, José de; Simpson, G M

doi:10.4088/jcp.v58n0603

Cited by 83 publications

(57 citation statements)

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“…However, the mechanism(s) involved in clozapine withdrawal phenomena and rapid relapse are not at all clear at present. They may involve "cholinergic rebound" after chronic treatment with an anticholinergic agent (Shore et al 1995;Shiovitz et al 1996;Verghese et al 1996;Stanilla et al 1997). In support of this analysis, it has been reported that clinical clozapine withdrawal effects can be treated with cholinergic antagonists (De Leon et al 1994).…”

Section: Introductionmentioning

confidence: 81%

“…Abrupt withdrawal from clozapine can be associated in some schizophrenic patients with rapid onset, timelimited withdrawal signs and symptoms, and also with rapid relapse and perhaps "rebound psychosis" (Ekblom et al 1984;Perenyi et al 1985;Alphs and Hong 1991;Parsa et al 1993;Keks et al 1995;Meltzer et al 1996;Shiovitz et al 1996;Stanilla et al 1997).…”

Section: Introductionmentioning

confidence: 99%

“…Reported clozapine withdrawal signs include nausea, vomiting, insomnia, diarrhoea, agitation, aggression, abnormal movements, headache and sweating (Keks et al 1995;Shiovitz et al 1996;Staedt et al 1996;Stanilla et al 1997); although psychotic signs of relapse such as delusions and hallucinations are also seen (Baldessarini et al 1995;Meltzer et al 1996;Still et al 1996;Stanilla et al 1997). Clozapine withdrawal signs and relapse to psychosis can be reversed by readministering clozapine (Perenyi et al 1985;Staedt et al 1996;Stanilla et al 1997).…”

Section: Introductionmentioning

confidence: 99%

“…Clozapine withdrawal signs and relapse to psychosis can be reversed by readministering clozapine (Perenyi et al 1985;Staedt et al 1996;Stanilla et al 1997).…”

Section: Introductionmentioning

confidence: 99%

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Clozapine as a drug of dependence

et al. 1999

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Clozapine induced a clear somatic withdrawal sign after chronic treatment. It is suggested that, in future research in both humans and animals, it is important to attempt to differentiate between clozapine withdrawal and clozapine withdrawal-induced relapse to psychosis. It is also important to characterise the clozapine withdrawal syndrome fully in animals; to establish the neurochemical mechanisms involved in such withdrawal; and to determine which novel antipsychotics are most efficacious in inducing clozapine-like withdrawal effects, in suppressing clozapine withdrawal, and in preventing relapse to psychosis in patients being transferred from clozapine to novel atypical antipsychotic drugs.

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Section: Introductionmentioning

confidence: 81%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…Clozapine withdrawal signs and relapse to psychosis can be reversed by readministering clozapine (Perenyi et al 1985;Staedt et al 1996;Stanilla et al 1997).…”

Section: Introductionmentioning

confidence: 99%

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Clozapine as a drug of dependence

et al. 1999

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“…Cases of withdrawal dystonias, dyskinesias and tics have been described with various antipsychotics (Tranter and Healy, 1996). Clozapine discontinuation symptoms usually commence within 2 to 3 days after stopping the drug and symptoms can include anxiety, insomnia, motor restlessness, delerium, nausea and diaphoresis (Borison et al, 1998;Eklund, 1987;Stanilla et al, 1997). Some patients who have been free of psychotic symptoms during clozapine treatment develop a rapid and florid psychosis within days of stopping clozapine (Ekblom et al, 1984).…”

Section: Antipsychotic Discontinuation Symptomsmentioning

confidence: 99%

Neurological complications of psychiatric drugs: clinical features and management

Haddad

Dursun

2007

Hum. Psychopharmacol. Clin. Exp.

190

106

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This paper reviews the main neurological complications of psychiatric drugs, in particular antipsychotics and antidepressants. Extrapyramidal syndromes include acute dystonia, parkinsonism, akathisia, tardive dyskinesia and tardive dystonia. Extrapyramidal symptoms (EPS) are less frequent with atypical than with conventional antipsychotics but remain common in clinical practice partly due to lack of screening by health professionals. Neuroleptic malignant syndrome (NMS) consists of severe muscle rigidity, pyrexia, change in conscious level and autonomic disturbance but partial forms also occur. NMS is particularly associated with the initiation and rapid increase in dose of high-potency antipsychotics but it has been reported with all the atypical antipsychotics and rarely with other drugs including antidepressants. Serotonin toxicity comprises altered mental state (agitation, excitement, confusion), neuromuscular hyperactivity (tremor, clonus, myoclonus, hyperreflexia) and autonomic hyperactivity and occurs on a spectrum. Severe cases, termed serotonin syndrome, usually follow the co-prescription of drugs that increase serotonergic transmission by different pathways, for example a monoamine oxidase inhibitor (MAOI) and a selective serotonin reuptake inhibitor (SSRI). Most antipsychotics and antidepressants lower the seizure threshold and can cause seizures; the risk is greater with clozapine than with other atypical antipsychotics and greater with tricyclic antidepressants (TCAs) than with SSRIs. In randomised controlled trials in elderly patients with dementia atypical antipsychotics are associated with a higher risk of stroke and death than placebo. Cohort studies suggest that conventional drugs carry at least the same risk. Cessation of treatment with antipsychotics and antidepressants can lead to a wide range of discontinuation symptoms which include movement disorders and other neurological symptoms. Clinicians need to be familiar with strategies to reduce the risk of these adverse events and to manage them when they arise. Their occurrence needs to be balanced against the benefits of psychiatric drugs in terms of efficacy and improved quality of life in a range of disorders.

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